Abstract
Finding new therapeutic targets to fight cancer is an ongoing quest. Because of insufficiencies in tumor vasculature, cells often are exposed to a hostile microenvironment that is low in oxygen (hypoxic) and nutrients. Thus, tumor cells face the challenge of finding new sources of energy and defying apoptosis, which allow them to survive, grow, and colonize other tissues. Eradicating specifically these hypoxic cells is one of the many goals of anticancer therapies. The mitochondrial voltage-dependent anion channel (VDAC) is a protein at the crossroads of metabolic and survival pathways. As its name suggests, VDAC is involved in ion transport as well as adenosine triphosphate and NAD+ transport. We recently reported the presence in tumor cells of a novel hypoxia-induced form of VDAC. This form, a C-terminal truncated protein (VDAC1-ΔC), was associated in some cancer cell lines with a high output of adenosine triphosphate and a strong resistance to chemotherapy-induced apoptosis. Furthermore, VDAC1-ΔC was detected in tissues of 50 % of 46 patients with lung cancer. This review examines the significance of this new form of VDAC1 for anticancer therapy.
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Acknowledgments
The laboratory is funded by the LigueNationaleContre le Cancer (équipelabellisée), the Association pour la Recherche contre le Cancer, the Institut National du Cancer, the AgenceNationale pour la Recherche, METOXIA (EU program FP7), the Centre A. Lacassagne, the Centre National de la Recherche Scientifique, the Institut National de la Santé et de la Recherche Médicale, and the University of Nice.
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Brahimi-Horn, M.C., Mazure, N.M. (2014). Hypoxic VDAC1: A Potential Mitochondrial Marker for Cancer Therapy. In: Koumenis, C., Hammond, E., Giaccia, A. (eds) Tumor Microenvironment and Cellular Stress. Advances in Experimental Medicine and Biology, vol 772. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-5915-6_5
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DOI: https://doi.org/10.1007/978-1-4614-5915-6_5
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